Cancers are diseases caused by multiple stages of gene mutations and have been found to occur due to the damage of some genes so that cells continue to increase without limitations. In normal cells, even if genes are damaged by the stress causing DNA damage, this damage is usually repaired by a repair mechanism. However, when cells are placed under strong stress, cell death called apoptosis occurs or cell cycle halts at a cell cycle checkpoint to irreversibly terminate cell growth. This phenomenon in which cell growth is irreversibly terminated is called “senescence” and considered as an important cancer inhibition mechanism comparable to apoptosis (Non Patent Literatures 1 to 4).
Unlike apoptosis, the occurrence of senescence does not immediately induce cell death, and instead, the cells continue to survive for a long period in vivo. Recently, it has been revealed that once senescence occurs, various inflammatory cytokines are secreted in large amounts (Non Patent Literatures 5 and 6). This inflammatory cytokine secretion phenomenon associated with the senescence is called senescence-associated secretory phenotype (SASP) or senescence-messaging secretome (SMS), suggesting the possibility that this phenomenon is one of the causes of chronic inflammation or carcinogenesis based on chronic inflammation (Non Patent Literatures 5 to 7).